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Case Report
10.4172/Neuropsychiatry.1000457 © 2017 p- ISSN 1758-2008
e- ISSN 1758-2016
Neuropsychiatry (London) (2017) 8(1), 758–766 758
Peritraumatic Dissociation and PTSD: a Shortcut to 
Neurodegeneration?
Patrícia Ferreira Mattos1,†, Adriana Mozzambani1, João Alencar Pedrini1, José Paulo Fiks1, Mario Francisco Juruena2, 
Marcelo Feijó de Mello1
1Universidade Federal de São Paulo, Rua Borges Lagoa, 570 - Vila Clementino, São Paulo - SP, Brazil
2Universidade de São Paulo, Catao Roxo, 2650- Ribeirão Preto, SP, Brazil
†Author for correspondence: Patrícia Ferreira Mattos, Rua Dr. Nicolau de Souza Queiroz, 406 apto 16, Vila Mariana, São Paulo- SP, Brazil, 
04005 001, Tel: +55 11 98381 5281, email: mattos.patricia@gmail.com
Abstract
Background: Peritraumatic dissociation has become increasingly important for both the 
diagnosis and the prognosis of Post-traumatic Stress Disorder (PTSD) and Acute Stress 
Disorder (ASD). Changes in inflammatory mediators, immune-related genes and alterations of 
the hypothalamic-pituitary adrenal axis are suggestive findings that support the role of stress 
and neurodegeneration that might result in negative cognitive outcomes, such as dementia 
and other comorbidities. This study aims to describe an ASD case with persistent peritraumatic 
dissociation, its evolution to PTSD and the concomitant early onset demential syndrome. 
Methods and Findings: The patient, a woman, victim of urban violence, experienced 
peritraumatic dissociation; she was diagnosed with ASD and later developed PTSD and 
concomitant EOD, the latter being an unexpected and devastating outcome. Dissociative 
symptoms and cognitive impairment persisted throughout the patient’s clinical status 
evolution. Moreover, the patient underwent a full psychiatric interview and was assessed 
through a battery of neuropsychological tests, neuroimage studies and a complementary 
examination. Over two years, no proposed treatment was satisfactory for improving her 
symptoms of PSTD and the neuropsychological evaluation confirmed EOD. 
Conclusion: This case illustrates that peritraumatic and persistent dissociation can be a 
possible psychopathological marker of neurodegeneration and an important factor for 
causing irreversible functional impairment.
Keywords
Peritraumatic dissociation, Dissociative symptoms, ASD, PTSD, Early onset dementia, 
Neurodegeneration
Introduction
Dissociative symptoms, predominantly 
peritraumatic dissociation, have become 
increasingly important for both the diagnosis 
and prognosis of Post-traumatic Stress Disorder 
(PTSD) and Acute Stress Disorder (ASD). 
Prospective studies [1,2] and meta-analyses 
[3,4] also indicate that dissociative reactions in 
the peritraumatic period would not only have a 
maladaptive character, but would also be a risk 
factor for developing later psychopathological 
manifestations.
The importance of dissociation in PTSD has 
been emphasized by many robust researches in 
the field [5,6] and there have been recurrent 
discussions if PTSD is best seen as an anxiety 
disorder or as a dissociative disorder [7,8]. 
Currently the Diagnostic and Statistical Manual 
please replace for: "severe cognitive alterations"
please replace for: "early onset demential syndrome"
Neuropsychiatry (London) (2017) 8(1)759
Case Report Patrícia Ferreira Mattos
stress axis would augment inflammation and 
have a direct effect on brain regions that are 
critical for processing fear and anxiety, such 
as the prefrontal cortex, insula, amygdala and 
hippocampus in chronic PTSD [15].
A range of evidence, in cross-sectional genetic 
and epigenetic studies, suggests that higher 
inflammation is associated with increased PTSD 
severity [16-18].
Other, reasons to believe that PTSD might be 
associated with accelerated brain aging is the co-
occurrence of depression, head injury, or medical 
comorbidities, all conditions associated with 
both PTSD and dementia. However, causal links 
between stress and PTSD and dementia, although 
suggested, have not been established [19].
Early Onset Dementia (EOD) or Presenile 
Dementia affects people under 65years of age and 
although it is considered a public health problem, 
it is still poorly documented and understood. It 
is underdiagnosed and inadequately treated, with 
limited services and resources in many countries 
[20]. Neurodegenerative diseases were the main 
causes of dementia in younger patients and they 
are more likely to have rare forms of dementia. 
EOD has a fast progression compared with Senile 
Dementia, with more extensive brain damage 
and complications [21]. There is a considerable 
delay of 2 to 3 years after the onset of symptoms 
to diagnose EOD, which can be explained by 
many factors: patients and family members do 
not normally consider the possibility of dementia 
at a young age, which delays seeking medical 
advice; clinicians, who are less likely to consider 
a diagnosis of dementia in young patients; the 
often prominent psychiatric manifestations and 
affected non memory cognitive domains [22].
This clinical case describes a patient with ASD, 
persistent peritraumatic dissociation, its evolution 
to PTSD and the concomitant early onset 
demential syndrome, provoking unexpected and 
devastating outcomes. This case illustrates the 
role of peritraumatic dissociation as an important 
predictor of PTSD and neurodegeneration and 
its fundamental implications for pathogenesis of 
trauma related conditions.
Methods and Procedures
The first psychiatric assessment occurred fifteen 
days after the traumatic event. This and all 
subsequent evaluations took place in a public 
mental health service from the Federal University 
of São Paulo (UNIFESP) specialized in the 
of Mental Disorders DSM-5 has classified PTSD 
in the new chapter of trauma- and stressor-related 
disorders and has included its dissociative subtype 
as a new feature [9]. Patients in this group would 
present predominant dissociative manifestations 
of depersonalization and derealization and would 
develop poor prognosis characterized by more 
severe functional impairment and psychiatric 
comorbidities, greater suicidality and history of 
early and multiple trauma [10].
Despite the growing interest in trauma and 
dissociation, this theme remains widely unclear. 
This phenomenon can be understood in several 
confusing and contradictory ways and there is not 
a universally accepted concept of dissociation. A 
review of 53 studies on PTSD and peritraumatic 
dissociation showed that none of them offered at 
least one definition of dissociation [11].
Dissociation can be considered as a process, 
an organization, a set of symptoms, or even as 
psychological defence mechanisms depending 
on the researcher theoretical position. Another 
element to factor in is if all dissociative symptoms 
represent the same neurobiological phenomenon. 
This question also remains unanswered [12].
Nevertheless, the link between peritraumatic 
dissociation/dissociative symptoms and a more 
severe dysfunctional evolution in post-traumatic 
conditions, draws attention to an understanding 
of the physio pathological pathways possibly 
involved in this process.
The physiological consequences of acute and 
chronic stress and trauma related conditions 
on several organs and systems have been well 
documented since the first studies of Hans Selye, 
almost 80 years ago [13].
More recently a focus on the possible long-
term “neurotoxic” effects of stressful life events 
has been proposed [14] and suggestive findings 
support the role of life stress, and PTSD in 
particular, in promoting negative cognitive 
outcomes, including worse than normal 
changes with aging, Alzheimer’s Disease, and 
Vascular  Dementia. The physiopathology of 
PTSD can be characterised from many different 
perspectives, including genetic, molecular, and 
neurochemical factors as well as neuro-circuitry 
and cognitive factors.
A possible mechanism that may link PTSD to 
higher rates of dementiacan be explained by the 
hypothalamic pituitary-adrenal axis alterations 
that often accompany PTSD until late in life. 
According to this model, dysregulation of the 
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Case ReportPeritraumatic Dissociation and PTSD: a Shortcut to Neurodegeneration?
treatment of victims of violence- “Program for 
Research and Assistance of Violence (PROVE).
The patient was informed about the research 
and signed the terms of consent approved by 
UNIFESP’s Research Ethics Committee and 
was submitted to a first interview utilizing a 
qualitative approach. PROVE provides support 
to patient’s victims of urban violence who had 
experienced acute traumatic events according to 
Criterion A of DSM-IV [23].
The psychiatric clinical evaluation was 
supplemented by the Clinician-Administered 
PTSD Scale (CAPS) [24], the Peritraumatic 
Dissociative Experiences Questionnaire, and 
Self-Report Version (PDEQ-SRV) [25] were 
deployed as complementary instruments. 
PDEQ-SRV is a self-administered questionnaire 
to track dissociative experiences that occurred at 
the time of exposure. A score above 15 indicates 
significant dissociation.
A Neuropsychological test battery was also 
applied by a team of PROVE neuropsychologists 
8 and 14 months after the traumatic event to 
assess the extent of impairment of cognitive 
functions. The tests were carried out because 
the patient had complained persistently of 
cognitive impairment. Inteligence: Wechsler 
Adult Intelligence Scale  (WAIS-III)  to measure 
intelligence [26]. Attention: Selective Attention 
Test [27], D2 Test of attention to  measure 
selective  and sustained attention and visual 
scanning speed [28], Color Trial: test to measure 
remote divided attention, sustained attention 
and the ability to achieve fine motor coordination 
suitable to the task [29], Divided and Alternating 
Attention Test [30]. Memory tasks: Wechsler 
Memory Scale Revised (WMS) to measure 
different memory functions [26]; Rey Auditory 
Verbal Learning Test [31], Rey Complex Figure 
Test. Test  (RCF), an assessment  in which 
examinees are asked to reproduce an intricate 
drawing, first by copying it (recognition), and 
then by drawing it from memory (recall) [32]. 
Executive functions: Verbal Fluency in which 
participants have to say as many words as possible 
from a category - semantic and phonemic- in a 
given time [33] and the Wisconsin Card Sorting 
Test  (WCST) a neuropsychological test which 
measures the ability to display flexibility in the 
face of changing schedules of reinforcement. 
Initially, a number of stimulus cards are 
presented to the participant; the participant is 
told to match the cards, but not how to perform 
this task; however, he or she is told whether a 
particular match is right or wrong [34]. It can 
assess strategic planning, organized searching, 
and the ability to utilize environmental feedback, 
direct behaviour toward achieving a goal, and 
modulate impulsive responding.
Neuroimaging studies, such as magnetic 
resonance imaging (MRI) and photon emission 
Figure 1: Patient’s evolution since the traumatic event: ASD, persistent peritraumatic dissociation, PTSD development and concomitant EOD as unexpected 
and devastating outcome.
progressive cognitive impairment
ASD PTSD 
Early
Onset
Dementia
15 d 1 m
traumatic
event
2 years
1st 
psychiatric
clinical
evaluation
8m 14m 
peritraumatic
dissociation persistent dissociation
1st
neuropsychol
tests
2nd 
neuropsychol
tests
Thyroid 
papiliferous
carcinoma 
12m 
delete "Test."
Neuropsychiatry (London) (2017) 8(1)761
Case Report Patrícia Ferreira Mattos
computerized tomography scans (SPECT) and 
complete blood count, lipids and hormonal test 
were also performed.
Case Report
Female, 50 years old, married, catholic, 
undergraduate sought the Care and Research 
Program of Violence (PROVE) of Federal 
University of São Paulo (UNIFESP) to receive 
psychiatrical assistance. She had no previous 
psychiatric history or any clinical comorbidities. 
She is a clinical social worker of a public health 
service. One of the patients assisted by that 
service lost his social benefit and consumed with 
rage, threatened her life, used his hand to mimic 
a gun and punched her on the mouth. At that 
precise moment, she sobbed and was completely 
out of control, subsequently feeling lethargic and 
sluggish. Some witnesses to the event said that 
she had hit the aggressor back, but she could not 
remember doing so. According to her, she felt as 
if she had not gone through that event.
Fifteen days after the traumatic event, she was 
still felling strange and fearful. She would tremble 
often and reported having constant chest pain. 
Before this first psychiatric evaluation, she had 
consulted with a cardiologist, as she believed she 
was having a heart attack. Since no cardiovascular 
alteration was found, the cardiologist referred 
her to psychotherapy.
She would feel unable to carry out her usual daily 
activities or go out on her own. She lacked the 
will to perform any simple task. Nothing would 
give her satisfaction. She described having an 
absence of feelings. She had intrusive thoughts 
about what happened and flashes of images 
where the aggressor´s face came back and forth, 
sometimes in the form of a hallucination. She 
was unable to even focus on easy tasks and often 
blundered while doing her daily activities. She 
mentioned that once, while cooking rice, she 
replaced oil with vinegar. On another occasion, 
she entered the wrong value while paying a bill. 
She was tired of having to watch over herself 
and felt devastated, especially worried about her 
thinking, memory, and attention conditions.
During the mental status examination, she was 
disoriented in time, presenting attention and 
memory impairment, which included amnesia 
of some part of the traumatic event. Her speech 
and mental processes were slow, marked by 
flashbacks and intrusive thoughts re-experiencing 
the traumatic event.
The patient featured intrusive symptoms, 
negative mood, dissociation, avoidance, and 
hyper arousal. Such symptoms are compatible 
with Acute Stress Disorder according to DSM-5 
and she scored 36 on PDEQ. Sertraline 25-50mg/
day was the recommended pharmacotherapy.
Evolution
One month past the event: She reported crying 
every day and stated that she had no energy 
during the day. She did not tolerate Sertraline; 
she had vomit and headaches and was afraid 
to take any medicine. She felt as if everything 
was happening in slow motion and she reported 
the same symptoms described in the first 
consultation, including the memory lapses. At 
that time, she fulfilled the PTSD diagnostic and 
scored 97 at CAPS. Sertraline was switched to 
Bupropione75mg/day as the initial dose. 
Two months later: She reported feeling better 
with Bupropion. She had stopped crying 
excessively and was able to do more than before, 
but unlike before, she needed to apply great 
effort to accomplish these tasks. She complained 
about many flaws in attention and memory and 
felt it was impossible to go back to work. She had 
inadvertently crashed her son´s car parked inside 
the garage. 
Six months later: She reported fewer intrusive 
thoughts, was more active and positive about 
her life as she received Bupropion 300mg/day. 
Although she had some improvement: she was 
able to think about the work with less sorrow, 
her daily life activities were still compromised; 
she was very distracted: she once misplaced the 
garbage, placing it into the refrigerator. She was 
fined for speeding and forgot many important 
appointments. She complained about insomnia, 
indifference, and lack of pleasure in all activities. 
She tried a cruise travel with her husband, but she 
could not feel the wellness that this experience 
used to provide to her. She tried to explain that 
with great difficulty: “I don’t know. I was there, 
something was happening, but I could not feel that 
happening. It’s a strange feeling, an empty feeling ...I cannot explain”
Agomelatine 25mg/ day was added, but the 
insomnia got worse and she became overactive, 
anxious, and irritable, doing many things 
automatically. Upon completing a task, she 
would have no feeling of fulfilment. She bought 
a new car, but that kind of happiness she usually 
felt was absent. For the risk of hypomania, we 
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Case ReportPeritraumatic Dissociation and PTSD: a Shortcut to Neurodegeneration?
suspended Agomelatine and she was given 
Bupropion 150mg and Citalopram 20mg/day. 
She was submitted to a Neuropsychological 
evaluation 8 months later.
One year later: She reported fewer intrusive 
thoughts, better thinking organization and less 
anxiety. Therefore, she could complete some 
regular tasks, and felt more functional. But 
she could not tolerate headaches caused by 
Citalopram and suspended medication herself. 
Desvenlafaxine 50mg was prescribed for a short 
period and rapidly interrupted. In that period, 
she was diagnosed with abnormal uterine 
bleeding (post menopause), which was attributed 
to antidepressant therapy by her gynaecologist. 
Shortly after, to her dismay, she was diagnosed 
with Thyroid papilliferous carcinoma.
She was very upset, and strived to avoid thinking 
about the thyroid cancer, as well as the traumatic 
event. She was submitted to total thyroidectomy 
and radioiodine therapy; she made a full recovery 
and had no further complications. Although she 
was treated with Duloxetine 120mg/day and 
Levothyroxin 100mcg/day, her cognitive deficit 
persisted. MRI showed no abnormalities. 
Two years later: The patient was extremely 
worried about her cognitive limitations. When 
she cooked, food would burn in the oven. She 
was very insecure and distracted to do any new 
task. On one occasion, while driving into her 
garage, she failed to break and drove into the 
gate, damaging both her car and the gate badly. 
Metilfenidate 10-30mg/day was prescribed, 
but she tolerated only 20mg/ day. Even though 
she reported having more energy and better 
disposition for her activities, she had attention 
and memory problems and her ability to carry 
out daily tasks was still very poor and limited. 
MRI showed no abnormalities, but SPECT scan 
demonstrated perfusion alteration of frontal 
lobes. At that time, she scored 106 at CAPS and 
the neuropsychological test battery was repeated. 
Patient’s evolution is summarized on Figure 1.
Neuropsychological Tests
The patient´s performance in each of the 
evaluated tasks was compared to norms for age 
and/or education. Her total estimated IQ scored 
at the high average range = 110, verbal IQ in the 
average range = 106 and the performance IQ in 
the high average range= 113.
At her first evaluation, 8 months after the 
traumatic event, she had severe impairment in 
the ability to focus and select stimuli, as well as 
difficulties to sustain attention and focus. The 
ability to alternate between tasks, i.e., sometimes 
keep the focus on a stimulus and then shift 
successfully to another one was in the 20% 
range, representing significant impairment. The 
ability to divide attention was in the lower range; 
her tasks had many perseveration and omission 
errors.
She had a borderline performance in 
more complex activities, involving mental 
manipulation of information (working memory). 
Her critical judgment was below average and 
she had substantial deficit in organization and 
planning capacity.
Analysis, synthesis, abstraction, verbal and 
logical reasoning were preserved, as well as 
executive and visual perception skills. Regarding 
language aspects, she presented higher than 
average performance in verbal understanding, 
displaying an extensive repertoire of words and 
excellent verbal fluency.
Memory tasks revealed that short-term memory 
and long-term auditory-verbal were moderately 
impaired. She performed better in visual memory 
tests, but still presenting significant deficits. 
Semantic memory was preserved.
In the second evaluation (6 months after the 
previous battery) tests were carefully applied to 
avoid the learning effect; word lists and memory 
tests were replaced by similar stimuli.
Attention still presented severe deficit in sustained, 
divided, alternating attention and focus. Selective 
attention declined dramatically, reaching an index 
below the average for the Brazilian population. 
Divided attention, remained in the lower range. 
The ability to alternate tasks remained in the 20% 
range. The D2 concentration test resulted in many 
omission errors.
Activities that examined working memory 
continued to show borderline performance, and 
organizational and planning deficits persisted. 
Compared with the previous assessment, the 
patient had decline in motor processing speed. 
Visual perceptual skills, language, abstraction, 
analysis, synthesis, logical and verbal reasoning 
were preserved. Short-term memory and long-
term auditory-verbal remained moderately 
compromised. Visual memory tests scores 
declined and semantic memory remained 
preserved.
Neuropsychiatry (London) (2017) 8(1)763
Case Report Patrícia Ferreira Mattos
Discussion
The criteria for ASD and PTSD diagnosis were 
met after 15 days and one month after the 
traumatic event, respectively. One can notice 
that the dissociative symptoms were present 
since the exact moment of the traumatic event 
and PEDQ scored 36. 
Among many dissociative symptoms, the patient 
emphasized that she was told that she had hit 
the aggressor back, but was completely unable to 
recollect this episode. On a day-to-day basis, she 
felt as if events in her life were not happening 
to herself and things seemed to be developing 
in slow motion. She was disoriented in time, 
lethargic and reported absence of feelings. 
Peritraumatic dissociative symptoms were listed 
as: amnesia, depersonalization, derealisation, 
time-space experience alterations and affective 
dissociation.
Dissociative psychopathology persisted 
throughout the patient’s clinical status evolution, 
but affective dissociation was her main complaint 
in almost every evaluation. The patient described 
it as indifference, lack of pleasure, absence of 
feelings, a strange felling, and an empty feeling. 
Those affective states had in common the fact 
that they were incoherent with the context 
meaning and disintegrated from her experience 
as a whole.
Even though DSM-5 recognizes dissociative 
symptoms in any form of PTSD, they are 
listed only as amnesia, depersonalization and 
derealization [35]. Cognitive, sensorimotor 
alterations and emotional or affective dissociative 
symptoms are poorly described or not described 
at all. Some signs of dissociation are merely 
described as a confusional mental state [36] or 
a transitory symptom which impacts diagnosis 
and treatment. This case is an example of how 
cognitive-emotional dissociative symptoms can 
emerge during and following adverse events and 
remain severe thereafter [37].
Since the 19th century and as early in the 21st 
century, dissociation has been recognized as the 
central mechanism leading to a whole spectrum 
of psychopathological conditions- such as 
PTSD, conversion and somatization, and affect 
regulation [38-41]. Psychosomatic diseases, 
autoimmune disorders and somatization have 
also been associated with trauma and dissociation 
[42].
However, there are many problems on 
conceptualization, classification and recognition 
of dissociative symptoms which may impact 
the diagnosis, treatment and prognosis of 
post-traumatic disorders [43]. In this clinical 
case, the concept of peritraumatic dissociation 
was considered a failure of synthesis of the 
emerging stimuli from internal and external 
world, including the time–space flow structure 
that encompasses the perceptual experience, 
even when the cognitive–perceptual tools are 
intact. This synthesis qualifies the totality of 
the perceptual experience as coherent and 
meaningful to the consciousness/self, enabling 
possibilities for being/existing[44].
After two years, although our patient reported 
some general subjective improvement, CAPS 
increased 9 points compared to her initial score. 
No antidepressant treatment was satisfactory 
for ameliorating the PTSD symptoms and the 
patient manifested intolerance to several drugs. 
Her best response was obtained with Bupropion, 
but still insufficient to the patient´s appropriate 
functioning. Metilfenidate also promoted a 
partial improvement of the patient’s cognitive 
symptoms, but the patient dysfunction was 
still very significant. Although all the available 
research data on biological findings in PTSD, 
there are no specific drug targets to treat this 
condition.
From the first evaluation up to two years 
following the traumatic event, the patient 
complained persistently about attention and 
memory impairment. Neuropsychological tests 
revealed cognitive decline in all attention aspects 
and visuomotor processing speed as well as 
compromised executive and memory functions. 
This case apparently has an abrupt onset and an 
identifiable emotional precipitant, which suggests a 
psychiatric rather than neurodegenerative diagnosis, 
but one can notice progressive impairment of 
cognitive functions over time, leading to an 
unexpected and devastating outcome: as an early 
onset demential syndrome. 
Psychological stress and stress-related disorders 
have been recognized as an increasingly 
widespread public health problem and women 
are twice as likely as men to suffer from stress-
related psychiatric disorders such as post-
traumatic stress disorder and clinical burnout 
syndrome [45,46].
It has been hypothesized that chronic stress 
conditions can lead to neural degeneration 
and Alzheimer Disease (AD) [46] and 
there are several neurohormonal pathways 
and genetic mechanisms to support this 
c
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Case ReportPeritraumatic Dissociation and PTSD: a Shortcut to Neurodegeneration?
Neurodegenerative diseases that target brain 
circuits involved in social and emotional processes 
create symptoms that mimic very closely those 
seen in psychiatric disorders and even highly 
experienced clinicians may be confounded.
Many neurodegenerative diseases indicate 
convergence with psychiatric syndromes and 
can be a powerful model system for studying 
the neural correlates of psychopathological 
symptoms. 
Notwithstanding, studies on neurodegenerative 
diseases have emphasized “cognitive” processes 
primarily (e.g., memory, visuospatial abilities, 
language, executive control, computation), and 
thus do not capture the emotional and social 
processes that are so relevant in psychopathology 
[50]. 
Conclusion
This case illustrates the importance of 
recognizing peritraumatic dissociation, a 
condition still poorly described and understood, 
as an important predictor of PTSD and as one 
possible harbinger of neurodegeneration causing 
irreversible functional impairment, such as an 
early onset demential syndrome.
Though suggested causal links between stress and 
PTSD and dementia have not been established, 
neurodegenerative conditions are the main 
causes of dementia in the pre-senile population. 
Thus, a full recognition of dissociation as 
psychopathological marker could be helpful to 
improve ASD and PTSD diagnoses and orient 
more effective treatment to comorbidities and 
consequences.
Proper investigation of 
neuropsychological  functioning may have 
important implications for the effective clinical 
management of patients with ASD and PTSD and 
must be considered even in dissociative states.
The neurobiological changes involving trauma 
and dissociation are only part of a plethora of 
pathologies pathologies that affect the whole 
organism and compromise brain, body and mind.
Acknowledgments
We thank to Universidade Federal de São Paulo 
(UNIFESP) and Coordenação de Aperfeiçoamento 
de Pessoal de Nível Superior (CAPES) to academic 
support and assistance and declare no conflict of 
interests.
association. Prolonged exposure to an excess 
amount of glucocorticosteroids at the time 
of a disadaptative  stress episode  would have 
deleterious effects on the hippocampus [47]. 
Indeed, the hippocampus plays a central role in a 
number of functions affected by dementia, such 
as memory, learning process and emotional 
adjustment. 
Severe dissociation has been correlated with 
slowness in processing information and 
distractibility. Depersonalization disorder 
(DPD), a dissociative disorder characterized by a 
subjective sense of unreality and detachment, has 
been linked to deficits in perception, short-term 
memory, cognitive disruption and attentional 
processes [48].
It is important to emphasize that PTSD 
should be conceptualised as a systemic 
disorder encompassing a range of biological 
dysregulations, including metabolic and altered 
immune function, reflected in the increased rates 
of cardiovascular and autoimmune disease. The 
risk of somatic comorbidities in PTSD appears 
to be confirmed as a consequence of changes in 
inflammatory mediators, immune-related genes 
and alterations of the hypothalamic-pituitary 
adrenal axis [49]. 
Thyroid papilliferous carcinoma was diagnosed 
one year after the trauma event. It is noteworthy 
that this patient had neither previous symptoms 
nor hormonal abnormalities or thyropathy 
family history. The patient was in psychotherapy 
throughout the follow-up period. Complete 
blood count, lipids and hormonal tests showed 
no abnormalities during this period. Alterations 
in the allostatic load involved in this process 
should be considered in the development of 
comorbidities in PTSD, which should be 
understood as a multisystem illness affecting the 
entire organism with somatic and neurological 
consequences.
There are numerous factors involved in the 
pathogenesis of dementia, but it is not clear 
if chronic stress or PTSD is both necessary 
and sufficient to result in dementia. Diseases 
and conditions identified as causes of EOD 
are mainly neurodegenerative ones, such 
as Alzheimer Disease, Vascular Dementia, 
Frontotemporal Lobar Degeneration, Dementia 
with Lewy Bodies, Traumatic Brain Injury, 
Alcohol-associated Dementia, Huntington’s 
disease, Parkinson’s disease Dementia, Mixed 
Dementia and Creutzfeldt- Jakob disease and 
Down’s syndrome [20].
delete
correct to : "conceptualize"
Neuropsychiatry (London) (2017) 8(1)765
Case Report Patrícia Ferreira Mattos
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